Bottom Line:
Carqueja (Baccharis trimera) is a native plant found throughout South America.CHE treatment also increased the defenses against β-amyloid toxicity in C. elegans, in part by increasing proteasome activity and the expression of two heat shock protein genes.Our findings suggest a potential neuroprotective use for Carqueja, supporting the idea that dietary antioxidants are a promising approach to boost the defensive systems against stress and neurodegeneration.

ABSTRACTCarqueja (Baccharis trimera) is a native plant found throughout South America. Several studies have shown that Carqueja has antioxidant activity in vitro, as well as anti-inflammatory, antidiabetic, analgesic, antihepatotoxic, and antimutagenic properties. However, studies regarding its antioxidant potential in vivo are limited. In this study, we used Caenorhabditis elegans as a model to examine the antioxidant effects of a Carqueja hydroalcoholic extract (CHE) on stress resistance and lifespan and to investigate whether CHE has a protective effect in a C. elegans model for Alzheimer's disease. Here, we show for the first time, using in vivo assays, that CHE treatment improved oxidative stress resistance by increasing survival rate and by reducing ROS levels under oxidative stress conditions independently of the stress-related signaling pathways (p38, JNK, and ERK) and transcription factors (SKN-1/Nrf and DAF-16/Foxo) tested here. CHE treatment also increased the defenses against β-amyloid toxicity in C. elegans, in part by increasing proteasome activity and the expression of two heat shock protein genes. Our findings suggest a potential neuroprotective use for Carqueja, supporting the idea that dietary antioxidants are a promising approach to boost the defensive systems against stress and neurodegeneration.

fig5: Effect of Carqueja hydroalcoholic extract (CHE) in transgenic C. elegans model for Alzheimer's disease. CL4176 transgenic strains treated or not with 50 mg/mL CHE were incubated for 40 h at 16°C. To initiate the β-amyloid-induced paralysis, the worms were up-shifted from 16°C to 25°C. The paralysis was verified each 2 h interval after 24 h at 25°C. The survival curves show that CHE alleviates β-amyloid-induced paralysis. (a) Paralysis profile of CL4176 transgenic animals fed with 50 mg/mL of CHE. **P = 0.0029 by the log-rank (Mantel-Cox) test. (b) Paralysis profile of CL4176 transgenic animals fed with 50 mg/mL of CHE mixed with KAN-treated bacteria. *P = 0.0353 by the log-rank (Mantel-Cox) test.

Mentions:
The observation that CHE has antioxidant properties in vivo led us to ask whether CHE treatment would have a protective effect against β-amyloid toxicity in a C. elegans model for the Alzheimer's disease. The expression of human Aβ1–42 in the muscle of transgenic CL4176 strain promotes a paralysis that can be monitored over time. We observed that the onset of paralysis was significantly delayed in 50 mg/mL CHE-treated animals (P = 0.0029). We observed that, after 24 h of induced Aβ1–42 expression, all CHE-treated animals were responsive to touch. After 32 h, this effect was still observed in 20% of the CHE-treated animals, compared to only 9% of the animals in the control group (Figure 5(a)). This effect was also independent of CHE antimicrobial effect. After 36 h, 50% of the CHE-treated animals were still responsive to touch, compared to 30% of the animals in the control group (P = 0.0353) (Figure 5(b)).

fig5: Effect of Carqueja hydroalcoholic extract (CHE) in transgenic C. elegans model for Alzheimer's disease. CL4176 transgenic strains treated or not with 50 mg/mL CHE were incubated for 40 h at 16°C. To initiate the β-amyloid-induced paralysis, the worms were up-shifted from 16°C to 25°C. The paralysis was verified each 2 h interval after 24 h at 25°C. The survival curves show that CHE alleviates β-amyloid-induced paralysis. (a) Paralysis profile of CL4176 transgenic animals fed with 50 mg/mL of CHE. **P = 0.0029 by the log-rank (Mantel-Cox) test. (b) Paralysis profile of CL4176 transgenic animals fed with 50 mg/mL of CHE mixed with KAN-treated bacteria. *P = 0.0353 by the log-rank (Mantel-Cox) test.

Mentions:
The observation that CHE has antioxidant properties in vivo led us to ask whether CHE treatment would have a protective effect against β-amyloid toxicity in a C. elegans model for the Alzheimer's disease. The expression of human Aβ1–42 in the muscle of transgenic CL4176 strain promotes a paralysis that can be monitored over time. We observed that the onset of paralysis was significantly delayed in 50 mg/mL CHE-treated animals (P = 0.0029). We observed that, after 24 h of induced Aβ1–42 expression, all CHE-treated animals were responsive to touch. After 32 h, this effect was still observed in 20% of the CHE-treated animals, compared to only 9% of the animals in the control group (Figure 5(a)). This effect was also independent of CHE antimicrobial effect. After 36 h, 50% of the CHE-treated animals were still responsive to touch, compared to 30% of the animals in the control group (P = 0.0353) (Figure 5(b)).

Bottom Line:
Carqueja (Baccharis trimera) is a native plant found throughout South America.CHE treatment also increased the defenses against β-amyloid toxicity in C. elegans, in part by increasing proteasome activity and the expression of two heat shock protein genes.Our findings suggest a potential neuroprotective use for Carqueja, supporting the idea that dietary antioxidants are a promising approach to boost the defensive systems against stress and neurodegeneration.

ABSTRACTCarqueja (Baccharis trimera) is a native plant found throughout South America. Several studies have shown that Carqueja has antioxidant activity in vitro, as well as anti-inflammatory, antidiabetic, analgesic, antihepatotoxic, and antimutagenic properties. However, studies regarding its antioxidant potential in vivo are limited. In this study, we used Caenorhabditis elegans as a model to examine the antioxidant effects of a Carqueja hydroalcoholic extract (CHE) on stress resistance and lifespan and to investigate whether CHE has a protective effect in a C. elegans model for Alzheimer's disease. Here, we show for the first time, using in vivo assays, that CHE treatment improved oxidative stress resistance by increasing survival rate and by reducing ROS levels under oxidative stress conditions independently of the stress-related signaling pathways (p38, JNK, and ERK) and transcription factors (SKN-1/Nrf and DAF-16/Foxo) tested here. CHE treatment also increased the defenses against β-amyloid toxicity in C. elegans, in part by increasing proteasome activity and the expression of two heat shock protein genes. Our findings suggest a potential neuroprotective use for Carqueja, supporting the idea that dietary antioxidants are a promising approach to boost the defensive systems against stress and neurodegeneration.